This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Helicobacter pylori are bacteria that infect the human stomach for decades, establishing intimate contacts with gastric mucous cells, and increasing the risk for gastro-duodenal ulcers and gastric cancer. The effector protein cagA is injected directly through a macromolecular 'syringe'from the bacterial cells into the host epithelial cells where it disrupts the junction barrier junction and causes loss of cell polarity and cytoskeletal control, and causes peptic ulcer disease and gastric carcinoma. We developed a cell-culture model of H. pylori chronic infection of MDCK cells where we co-culture virulent H. pylori with epithelial cells for periods of hours to months and monitor bacterial-cell interactions. Our recent physiological results indicate a capacity of H. pylori to extract iron from the surrounding epithelial cells upon attachment and expression of cagA effector protein, whereupon cell polarity is altered. Iron absorption, and probably also Nickel and Zinc, seem to be intimately involved in the successful colonization of the host epithelial cell.